There are a number of dental disorders that result in the resorption of alveolar bone. Probably the most important of these is periodontal disease (PD) which leads to bone loss in 30 - 100% of the population in the United States above the age of 35. Bone resorption is generally associated with increased numbers and increased activity of osteoclasts. Unfortunately, for a number of technical reasons the origin and fate of these and other bone cells is still incompletely understood. Recently, we have developed a new experimental system for the study of bone cell lineage that involves the establishment and growth of quail (chimeric) bone rudiments on the chorioallantoic membrane (CAM) of chick embryos (Kahn and Simmons, 1975). This system has two advantages over those previously employed. First, because of inherent differences in nuclear morphology, bone cells of quail origin can almost always be distinguished from those derived from the chick. Second, because CAM grafts are vascularized by an extrinsic blood supply, it is possible to determine if, and under what circumstances, osteoclasts and osteoblasts may originate from cells of the blood vascular system. We propose to utilize this system to examine the response of osteoprogenitor cells, osteoclasts and osteoblasts: (a) to agents such as PGE2 and endotoxin that are associated with PD: (b) to bone-effecting hormones like PTH, calcitonin, estrogen; (c) during fracture healing; and (d) during bone modeling and remodeling.